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The Triad Learning Objectives bruxism, sleep disturbance, and sleep-related GERD. • describe a normal and list By Jeffrey S. Rouse, DDS three sleep disturbances, including the testing parameters for each.

• list the factors involved in the bruxism tribological interaction. Friction is en- triad and understand the influence Abstract countered whenever there is relative of each. Sleep bruxers are a difficult subset of patients to manage predictably. They damage motion between contacting surfaces, teeth and restorations at a higher rate than normal -related bruxers. The adverse and it always opposes the motion. As • discuss treatment options for patients effect of their sleep bruxism does not stop just with damage.T hese patients are no surface is perfectly smooth, when diagnosed with the bruxism triad. more prone to sleep disturbances including and gastric reflux symptoms. It the teeth make contact, even under appears that these three sleep issues are interwoven in a triad of factors that create Log on to www.insidedentistryCE.com a uniquely detrimental environment for teeth. light load, it may produce the loss of tooth structure. When non-roughened to take the FREE CE quiz. surfaces contact, their coefficient of fric- ruxism is defined as points to neurochemistry, autonomic tion decreases dramatically if a lubricant a diurnal and noctur- system, and sleep arousals as possible is introduced. Tribology would suggest wrote that the bite strength in some nal parafunctional triggers.7,8 This article will restrict its that a decrease in oral lubrication cou- bruxer-clenchers can be as much as activity that includes focus to a unique subset of the brux- pled with tooth-on-tooth contact would six times that of the non-bruxer.15 The clenching, bracing, ing population: the sleep bruxer. This introduce friction and, thus, wear.12 In study evaluated daytime bite strength, gnashing, and grinding group is extremely destructive to their addition, elements that increase the not nocturnal bruxing force. It also did of teeth.1 The damage teeth and systemic health. Additionally, surface roughness (eg, erosion) would not provide groups for bruxing subjects from bruxism is a reality in the everyday this article will discuss the significance unavoidably increase wear (Figure 2). and a non-bruxing control. In fact, the Bpractice of and yet there is a of the bruxism triad: sleep bruxism, Intraoral lubrication is provided pri- conclusion of the study should have great deal of and controversy. sleep disturbance, and sleep-related marily by saliva. It also lubricates and read that only one patient in the study Dental professionals do not even agree gastroesophageal reflux. buffers the esophagus and decreases during the day could produce six times on the relative number of people who the risk of aspiration.12 Salivary flow fol- greater force on biting than the aver- brux. The estimates range from 5% to lows a daily circadian variation and is age dentate patient. Studies monitor- 95% of the population.2-4 Many Tooth wear is described in the litera- significantly lower at night.D uring sleep, ing muscle activity during sleep have focus on the patients who present with ture as the loss of the constitution of the deglutination is episodic, with long peri- confirmed that the elevator muscles wear to determine rates of bruxism. tooth and has been classified as being ods without swallowing. Daytime swal- are rarely, if ever, contracted to their Tooth wear, however, is a poor indica- caused by attrition, abrasion, erosion, lowing averages 25 to 60 times per hour maximum. In fact, when the EMG tor of bruxism since attrition may play or a combination of these factors.9 As it and only two to nine times at night.13 levels are evaluated during nocturnal only a small role in tooth destruction relates to SB, tooth wear is reported to Salivary flow and buffering capacity vary bruxing activity, the muscle response and may not be indicative of an ongoing additionally cause tooth mobility, tem- between individuals and may be insuf- is only half of the maximum voluntary problem.5 The smaller estimates limit perature hypersensitivity, and tooth ficient to prevent frictional tooth dam- contraction.16,17 Only 66% of the brux- the patients to sleep bruxers. Sleep fracture.10 While sleep bruxers and age.14 Swallowing is almost exclusively ism episodes are at a force level equal bruxism (SB) is the grinding or clench- non-bruxers displayed significantly dif- associated with microarousals (MA) to or greater than the force generated ing of the teeth during sleep, usually as- ferent amounts of wear over time, the during light sleep.13 These MAs play an during . While it is true that pa- sociated with sleep arousals.6 To date, contribution of tooth-on-tooth attri- important role in sleep bruxism. tients with greater jaw muscle size may the pathophysiology for SB has not tion to this wear is still controversial.11 Reduced lubrication, erosive friction, generate more total force with the same been definitively determined.R esearch It has been postulated that much of the and contact time play significant roles EMG activity, the amount of force is wear could be erosion rather than at- in tribologic wear of teeth in sleep brux- well within daily norms and definitely Jeffrey S. Rouse, DDS trition. Interestingly, those two factors ers. Bruxing force is not as important as not six times greater. Private Practice are interwoven in the bruxism triad previously thought. For years the pro- Prosthodontist patient, magnifying the wear in this fession has accepted that SB patients Sleep Stages and Clinical Adjunct patient population (Figure 1). can exert up to six times as much force Arousal Response Associate Professor The study of tooth wear is appropri- on their teeth at night than normal sub- Good-quality sleep is important for Department of Graduate 15 ately described as tribology: the science jects. It has provided dentists a simple physical recovery, biochemical re- University of Texas Health of interacting surfaces in relative mo- explanation to our patients as to why freshment, , and Science Center San Antonio tion and associated issues of lubrication, their teeth wear and restorations break. emotional regulation.18 A typical sleep Dental School friction, and wear. Teeth sliding over Interestingly, the facts simply do not cycle is 90 to 110 minutes of sleep with San Antonio, Texas each other are affected by a complex support that conclusion. Gibbs et al three to five cycles per night. Sleep is

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composed of two distinct states: non- vibration induced by air turbulence. It more than 3%. The level of OSA is re- and decreases with age. SB occurs in up REM (quiet sleep) and REM (active is reported in 40% of men and 24% of lated to the number of apnea- to 30% of children from 5 to 6 years old, sleep). There are four stages of non- women. The incidence is 10% in chil- events per hour of sleep. The apnea-hy- 13% in respondents 18 to 29 years of age, REM sleep. Stages 1-2 are light sleep dren.22 is a risk factor for ob- popnea index (AHI) considers persons and decreasing to 3% in patients over and Stages 3-4 are deep sleep. In the structive (OSA). A medical with 5 to 15 events per hour of sleep as 60 years old.28 Unlike stress-triggered first third of total sleep, non-REM consultation is appropriate before mak- mild, 15 to 30 as moderate, and > 30 as bruxing subjects, sleep bruxing episodes Stage 3-4 is the longest stage and de- ing an oral appliance for snoring and is severe. The severity of sleep apnea is are unrelated to experienced and antici- creases or disappears in the last third. mandatory when snoring is accompa- judged by a composite of the symptoms pated stress.29 In addition, SB has little REM sleep increases in the last third. nied by daytime sleepiness, , including AHI, daytime sleepiness, and variability in the bruxing episodes and While may occur in any stage sleep disruption, or . % desaturation. Risk factors for OSA in- bursts per hour of sleep over months of sleep, they are more common and UARS is an increased inspiratory clude being male, , over 40, and years.30 In moderate to severe SB, more vivid in REM sleep.20 effort creating increased MAs and nar- large size, large , and family grinding was present every night.31 A micro-arousal (MA) is a shift in sleep rowing of the without oxygen history (Figure 3).24 It is estimated that Sleep bruxism episodes are related occurring during deeper sleep. These 3- desaturation below 4%.23 It is character- 1 in 5 adults has at least mild obstructive to disturbances in sleep. Kato and col- to 10-second rises in EEG activity cre- ized by repetitive partial collapse of the sleep apnea (OSA) and 1 in 15 has at leagues induced MAs during the sleep ate an increase in heart rate and muscle upper airway during sleep. UARS have least moderate.25 Unlike the bruxism of sleep bruxers and controls.32 Tooth tone. MAs occur 8 to 15 times in an hour. been linked with increased bruxism, , OSA increases with age grinding followed the experimentally Bruxism is an oromotor manifestation , and TMD, and are thought and can affect 70% of men and 56% of induced MA in more than 71% of the secondary to MA. Eighty-six percent to be an intermediate form of disorder women over the age of 65, a three-fold trials. Interestingly, this reaction was of bruxism occurs in non-REM Stage 2 between snoring and OSA.22 increase from middle age.26 While be- only produced in sleep bruxism pa- sleep and MA.19 A smaller percentage of Apnea is the repetitive absence of yond the scope of this article, OSA is a tients and never in controls, indicating bruxism events occur in REM sleep.20 ventilation with cessation of risk factor for hypertension, cardiovas- a heightened responsiveness to sleep More destructive bruxers, however, have for 10 seconds and oxygen desaturation cular morbidity, and daytime sleepiness arousals. Therefore, anything that in- a greater number of episodes and time of exceeding 4%. Sleep apnea may be ob- to name just a few.25 duces a greater number of MAs has the bruxism in REM sleep than controls.21 structive sleep apnea (most common) ability to increase the amount of tooth resulting from a blockage of the upper Sleep Bruxism grinding in these subjects. Sleep Disturbances airway or demon- A sleep bruxer is different than a pa- Respiratory disturbances during sleep strated by no chest movements result- tient who occasionally bruxes during Airway fall into three categories: snoring, upper ing from a lack of neural drive.18 Patients sleep. By definition, a sleep bruxer must Researchers observe that the frequency airway resistance syndrome (UARS), may have both types simultaneously. have > 4 episodes of bruxing per hour of sleep apnea increased as the frequency and sleep apnea-hypopnea syndrome. Hypopnea is a decrease in airflow of of sleep, > 25 bruxing bursts per hour, of bruxism increased. Given the link be- Snoring is defined as sounds produced more than 50% or a decrease of airflow and at least one episode per night must tween MA and SB, it may be more cor- in the upper airway from soft tissue by 30% with an oxygen desaturation of make noise.27 SB is higher in children rectly stated that the frequency of SB

fig. 1

fig. 2

CLINICAL EXAMPLES (1.) Classic presentation of the bruxism triad. Lateral wear pattern, generalized buccal from erosion and abrasion, and history of sleep disruption. (2.) Asymmetric tooth wear in a bruxism triad patient as a result of friction from bruxing, poor salivary lubrication as a byproduct of medication, and roughened surfaces created as a result of erosive reflux. (3.) In addition to the traditional sleep apnea risk factors (over 40 years old, male, overweight, >17 inch neck size), practi- tioners should add the tooth wear and erosion components of the bruxism triad.

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in 20- to 40-year-old subjects may sim- ply be an attempt to open their airway. As the sleep bruxer ages, their neuro- chemical ability to brux decreases, or it cannot overcome the additional airway obstructions due to a loss of muscle tone, , etc.

fig. 4 fig. 7 fig. 10 GERD Gastroesophageal reflux disorder (GERD) is a medical condition where the stomach contents leak to the esoph- agus. It affects approximately 40% of Americans.39 GERD is commonly as- sociated with heartburn or indigestion, although > 50% of people complain- ing of frequently clearing their throat, hoarseness, or trouble swallowing were fig. 5 fig. 8 fig. 11 found to have silent GERD. Poor qual- ity of sleep may be the sole presenta- tion of silent GERD in asymptomatic subjects.40 Medical consultation is recommended. would include peptic ulcer, , and Barrett esophagus (possible precursor to adenocarcinoma).41 Some of the acid content of the stom- ach may reach the oral cavity. This is an fig. 6 fig. 9 fig. 12 extremely destructive acid with a pH of 1 to 2. In comparison, dietary acids are SYMPTOMS OF THE TRIAD (4.) RESULTS OF THE TRIAD (7.) Patients Recognizing Triad Patients Indentations on tongue caused who combine tongue pressure to (10.) Extensive wear on stabilizing greater than pH 3. The most common by forceful pressing of tongue clear the airway and GERD can splint. It has been postulated that site for damage is the palatal surface on lingual surfaces. By pushing produce wear on the lingual sur- continued bruxism on splints is patho- of the maxillary molars (Figure 5 and the tongue anteriorly, the airway faces resembling bulimia. It is not pneumonic for the bruxism triad. (11.) is opened. (5.) The red, irregular restricted to maxillary anteriors. (8.) Continued wear on splints is indepen- Figure 6). Reflux symptoms present surface on the palatal surface of a Young adult with signs and symp- dent of the design of the . mostly in a supine position. The dor- maxillary molar can be an early sign toms of the bruxism triad: Lateral Childhood presentation of the (12.) sum of the tongue pushes the acid to the of reflux.(6.) Continued damage tooth wear, erosive and abrasive bruxism triad. Patient had erosive from erosion produced by GERD. damage to the teeth, and a history and attritional wear on deciduous maxillary molar palatal surface when Other areas of erosive damage will of moderate apnea. (9.) Extensive teeth, constricted dental arches, and swallowing to buffer the acid.42 While be dictated by the sleep posture of erosive wear. Airway improvement deep class II bite. Physician examina- the patient. can reduce GERD and GERD resolu- tion revealed significant GERD paired the palatal surface is the most common tion can reduce sleep bruxism. with enlarged and tonsils. site of destruction, the pattern of dam- age will be dictated by the sleep posi- increases with an increase in sleep apnea- episode. The majority of SB episodes Bruxism is greatest in 5- to 6-year- tion of the patient during the episodes. induced arousals.22,33 At least one third of occurs in a supine position and may be olds and slowly declines with age. Ad­ Tongue activity associated with airway patients with bruxism in the general pop- associated with either a reduction in the enoid hypertrophy in the 5- to patency coupled with regurgitation may ulation may also have sleep-disordered airway passage or increase in its resis- 6-year-old patient may account for the also create wear on the lingual surfac- breathing conditions such as sleep apnea, tance. During resumption of ventilation and, thus, a greater es of teeth resembling bulimia but are periodic leg movement during sleep, and following apnea, a co-activation of both incidence of bruxism.28 As the airway not limited to the maxillary anteriors .22,34 The rate of OSA may be as jaw-opening and jaw-closing muscles improves with age, the bruxism decreas­ (Figure 7). GERD patients have a sig- high as 30% in a TMD population.(18, unpub- produce dilation of the upper airway. es in the general population but in the nificantly higher risk of and lished data) In addition to OSA, close to 50% This permits a rise in inspiratory flow triad group it continues. If bruxism is oral burning sensation.43 This lack of lu- of UARS patients complain of bruxism.22 and reduces upper airway resistance.37 a reflexive mechanism to improve or brication paired with acid-roughened Prospective evaluations and case studies It has been reported that 99% of all protect an airway, then greater brux- surfaces increase the risk of frictional of SB and apnea indicate that bruxism rhythmic masticatory muscle activi- ism could lower the apnea. Sjöholm con- wear associated with sleep bruxism. events may be directly correlated to ap- ties were associated with a change in the cluded that there is limited correlation nea episodes.35 While a causal relation- respiratory amplitude and frequency.19 between bruxing and apnea because Bruxism Triad: Sleep ship cannot be made, obstructive sleep Changes in lateral tongue contours, mild apnea patients had more bruxing Bruxism, Sleep Disturbance, apnea (OSA) syndrome has been called long associated with nocturnal brux- events than moderate apnea patients.38 and Sleep-Related GERD the highest risk factor for tooth grinding ers, can now be explained. The patient However, if bruxism is a protective re- The bruxism triad coupled with noctur- during sleep.36 attempts to provide a patent airway by flex, clinicians might be able to predict nal hyposalivation or xerostomia appre- Bruxism and airway appear to be re- activating the tongue muscles and forc- the possibility in a young patient popu- ciably increases the risk of frictional and lated to the patient’s attempt to develop ing the tongue off the airway and against lation that bruxism would be linked to erosive tooth wear.12,18 The bruxism triad a patent airway during a desaturation the teeth (Figure 4). less severe apnea. Aggressive bruxism is composed of arousal-induced tooth

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grinding, airway-associated sleep disor- GERD.49 While the link is still contro- a mandibular posterior inclination, occlusal orthosis. Continued grind- ders, and sleep-related GERD (Figure 8 versial, one explanation is that during greater anterior face height, and ret- ing on the appliance is a hallmark for and Figure 9). While a causal relation- apnea episodes, there is an increase in roclined incisors (Figure 12).55 the bruxism triad. Self-reports of high ship has not been established, significant negative intrathoracic pressure. This in- stress may be due to repeated sleep dis- correlation makes it important for den- creased negative pressure could cause Adolescent 13–19 turbance and should not be disregarded. tists to evaluate their patient population. the gastric acids to be expelled from the Dentists commonly tell parents that Evidence of GERD may be present on Sleep bruxism is concomitant with stomach and into the esophagus. As the most children “grow out of bruxism” the teeth or maxillary palatal tissue. sleep apnea. Therefore, if the level of ap- esophageal pH decreases, patients’ brux- when they reach . More accu- Bruxism may be acting as a protective nea can be artificially reduced, a resul- ing episodes were significantly higher. rately, many children grow enough to reflex for the airway (Figure 14). There tant decrease in bruxism would be an- Miyawaki studied 10 SB and 10 controls overcome the impact of the adenoids is a statistically significant association ticipated. Oksenberg and Arons found presenting without GERD symptoms. and tonsils, or orthodontic intervention between childhood wear of the decidu- that during continuous positive airway Esophageal pH was monitored during expands the palate enough to create an ous mandibular molars and canine teeth pressure (CPAP) treatment, an evening of sleep. Results showed adequate airway. Any signs of patho- and the degree of whole-mouth wear ob- were eliminated and only a few hypop- that when the esophageal pH reached logic wear due to attrition or erosion at served 20 years later56 (Figure 15). For neas were seen. A complete disappear- 4 or lower there was a simultaneous this stage should elicit questions about sleep bruxers with episodic sleep distur- ance of all bruxism events occurred.35 bruxism episode ending in a tonic burst sleep disturbances, sleep bruxing, and bances and reflux symptoms, this author Mandibular advancement appliances representing a swallow.50 This is appar- reflux symptoms (Figure 13). has been using an anterior reposition- (MAA) have reported to reduce bruxism ently an attempt to buffer the esopha- ing splint with success. The appliance events 50% to 83%.44 The variability geal acid content. Interestingly, the pH Young Adult 20–40 is fabricated at < 40% of the patient’s appears to be related to the appliances’ 4 threshold was reached exclusively by Pathologic tooth wear or significant maximum protrusion, minimizing the ability to reduce desaturation episodes, SB patients. No control patient had an relapse of orthodontic correction is occlusal risk associated with advance- which is more inconsistent than CPAP esophageal pH low enough to trigger a usually addressed by fabrication of an ment appliances (Figure 16 and Figure therapy. The MAA may also be used in bruxism episode. SB patients without respiratory distur- Proton-pump inhibitors are a group of bances. A statistically significant reduc- that reduce gastric-acid production. tion (39% and 47%) of SB episodes per Administration of a proton-pump inhibi- hour was recorded with the MAA at pro- tor to GERD-SB patients demonstrated trusion of 25% and 75%, respectively,45 a commensurate 40% reduction of SB providing further evidence that im- episodes.50 Another family of GERD proving airway patency is an important medication, the H2 blocker anti-acids, treatment strategy for bruxism even in showed a reduction in MAs, respiratory a normal patient population. disturbances, and daytime . fig. 13 fig. 14 One important note is that traditional It did not, however, reduce the AHI.51 occlusal stabilizing splints may have a Reducing the intrathoracic pressure with deleterious effect on SB-OSA patients. CPAP reduces GERD parameters in pa- A prospective study of 10 mild to mod- tients with and without OSA.51,52 Studies erate OSA patients was conducted with with MAA have not been conducted but multiple nights recorded with and with- similar results would be anticipated giv- out a stabilizing splint. Results indicated en their impact on the airway. that six of the 10 subjects had a signifi- cant increase in their AHI with splint Recognizing the Triad Patient therapy.46 Further, OSA patients with Dentists should to be able to recognize complete have significantly the bruxism triad patient at all stages fig. 15 improved airways when sleeping with of life. Early diagnosis can alter poor their dentures than without them.47 Both growth, improve physical well-being, studies highlight that OSA patients have and reduce tooth wear. The following an improved airway when the are some of the distinguishing features is placed and held in a protruded posi- of each of the stages of the triad. tion. Efforts which prevent that abil- ity may worsen the airway and increase Childhood 3–12 sleep bruxism. This could account for and tonsil hypertrophy pro- fig. 16 fig. 17 the severity of wear found on some oc- duces sleep disturbances including clusal splints. The author has noted that OSA. The magnitude of hypertrophy Early Signs and Treatment (13.) Adolescent triad: A 16-year-old with patients with airway and GERD issues required for obstruction is smaller in pathologic wear on incisors and a loss of tooth texture from erosion and abrasion. Medical history was indicative of the triad. (14.) Bruxism triad in have notably more wear on their orthosis obese children compared to non-obese a young adult. The pathologic wear, once limited to the anterior teeth, is regardless of design (Figure 10 and 11). children.53 GERD will be found fre- beginning to appear on the posteriors as guidance is lost. Patient reported GERD can be linked to the other mem- quently in children with adenotonsil- sleep issues that became exacerbated with . GERD was inter- mittent until pregnancy then it increased. (15.) Patient demonstrates wear bers of the triad. Patients with GERD lar hypertrophy and OSA and should on deciduous molars increasing the risk of bruxing as an adult. Another had higher AHI scores and shorter pe- be evaluated.54 Five-year-old children explanation may be the triad. Constricted dental arch, crowded lower ante- riods in restful Stage 2 sleep.48 Research with OSA will commonly display dif- riors, and a deep bite with a lifetime of airway-related issues. GERD history coupled with erosive wear on teeth. (16.) Ramp of the anterior repositioning has also demonstrated that more severe ferences in growth when compared to appliance demonstrating the path of the incisors from centric closure to OSA was accompanied by more severe matched controls. This can include anterior closure. (17.) Patient positioned at 40% of voluntary protrusion.

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17). The maxillary orthosis directs the Medical issues related to overall health nature of bruxism, breathing, and ero- occlusal wear in an adult Swedish population. patient’s closure into a protruded pos- may be linked to OSA. Bruxism may be sion. These patients suffer a significant Acta Odontol Scand. 1990;48:343-349. ture that opens the airway without being present but will be limited in its ability loss of tooth structure and restoration 6. American Academy of Sleep . as bulky and restrictive as most MAAs. to clear the airway and reduce GERD. damage due to the increase in friction International Classification of Sleep Disorders. 2nd Patients may need to address tooth due to poor lubrication and roughened ed. American Academy of ; 2005. Middle Adult 40–65 wear issues that have been compound- surfaces. Medical evaluation is key. 7. Lavigne GJ, Manzini C. Bruxism. In: Kryger Bruxism will begin to wane as the risk ed through years of neglect (Figure 21 CPAP, MAA, and GERD medications M, Roth T, Dement W (eds). Principles and of OSA increases. The impact of tooth and Figure 22). Comprehensive evalua- were proposed as possible treatment Practice of Sleep Medicine. 3rd ed. Philadelphia, grinding may be reduced but medical tion for of OSA and options for the bruxism triad patient. Pa: W.B. Saunders Company; 2000:773-785. complications of OSA and GERD have referral for polysomnographic study is 8. Lavigne GJ, Kato T, Kolta A, Sessle BJ. increased. The effects of years of tooth recommended. Patients with dentures References Neurobiological mechanisms involved in sleep and restoration damage may be ap- should be encouraged to wear their 1. De Leeuw R. Orofacial Pain Guidelines for bruxism. Crit Rev Oral Biol Med. 2003;14:30-46. parent. Airway management becomes dentures at night if sleep disruption is Assessment, Diagnosis, and Management. 4th ed. 9. Litonjua LA, Andreana S, Bush PJ, Cohen more difficult given the physical chang- present (Figure 23 and Figure 24). Chicago, Ill: Quintessence; 2008. RE. Tooth wear: Attrition, erosion and abrasion. es of middle age (Figure 18). As the lit- 2. Lavigne GJ, Montplaisir JY. Restless leg Quintessence Int. 2003;3:435-446. erature elucidated, management of the Conclusion syndrome and sleep bruxism: Prevalence 10. Lavigne GJ, Manzini C, Kato T. Sleep airway during sleep improves all factors It has been demonstrated that a ma- and associations among Canadians. Sleep. Bruxism. In: Kryger M, Roth T, Dement W (eds). of the triad. CPAP is the gold standard jority of dental patients present with 1994;17:739-743. Principles and Practice of Sleep Medicine. 4th for airway maintenance. For patients tooth wear. However, sleep bruxers are 3. Ohayon M, Li KK, Guilleminault C. Risk fac- ed. Philadelphia, Pa: W.B. Saunders Company; unwilling or unable to use CPAP, MAAs a unique subset. Sleep bruxism is reflec- tors for sleep bruxism in the general population. 2005:946-959. have the potential to diminish AHI, re- tively triggered by sleep microarousals. Chest. 2001;119:53-61. 11. Pintado MR, Anderson GC, DeLong R, duce sleep bruxism, and potentially These disturbances in the sleep pat- 4. Okeson JP, Kemper JT. In: Okeson JP. Man­ Douglas WH. Variation in tooth wear in young lessen GERD (Figure 19 and Figure 20). terns are a natural occurrence but can agement of Temporomandibular Disorders and adults over a two-year period. J Prosthet Dent. also be caused by any disruption of air- . 5th ed. St Louis, Mo: CV Mosby; 2003. 1997;77:313-320. Mature 65 Older way patency or a significant reduction 5 Ekfeldt A, Hugoson A, Bergendal T, Helkimo 12. Thie NMR, Kato T, Bader G, et al. The The majority of patients in the mature of esophageal pH. The bruxism triad is M. An individual tooth wear index and an significance of saliva during sleep and the group will have at least mild apnea. an attempt to explain the interlocking analysis of factors correlated to incisal and relevance of oromotor movements. Sleep Med Rev. 2002;6:213-227. 13. Lichter I, Muir RC. The pattern of swal- lowing during sleep. Electroencephalogr Clin Neurophysiol. 1975;38:427-432. 14. Moazzez R, Bartlett D, Anggiansah A. Dental erosion, gastro-oesophageal reflux and saliva: how are they related? J Dent. 2004;32:489-494. 15. Gibbs CH, Mahan PE, Mauderli A, et al. Limits of human bite strength. J Prosthet Dent. 1986;56:226-229. fig. 18 fig. 19 fig. 20 16. Clark NG, Townsend GC, Carey SE. Bruxing patterns in man during sleep. J Oral Rehabil. 1984; 11;123-127. 17. Nishigawa K, Bando E, Nakano M. Quan­ titative study of bite force during sleep associated bruxism. J Oral Rehabil. 2001;28:485-491. 18. Lavigne GJ, Cistulli PA, Smith MT (eds). Sleep Medicine for Dentists: A Practical Overview. Chicago, Ill: Quintessence Publishing Co, Inc; 2009. fig. 21 fig. 22 fig.23 19. Khoury S, Rouleau GA, Rompré PH, et al. A significant increase in breathing amplitude pre- Middle-adult triad patient. Pathologic wear from Advanced Triad (18.) cedes sleep bruxism. Chest. 2008;134:332-337. sleep bruxism and erosion damage on multiple tooth surfaces. Patient had a history of GERD treated with a proton-pump inhibitor medication. Patient 20. Baba K, Clark GT, Watanabe T, Ohyama reported a decrease in bruxism but partner noticed an increase in snor- T. Bruxism force detection by a piezoelectric ing and apnea events. revealed an AHI of 34. Thorn- (19.) film-based recording device in sleeping humans. ton Adjustable Positioner 3 (TAP). Custom made MAA for the treatment of sleep disturbances. Anterior connector allows adjustment for titration of J Oral Pain. 2003;17:58-64. the airway. (20.) TAP 3 engaged. (21.) Mature patient with the bruxism triad. 21. Okeson JP, Phillips BA, Berry DT, et al. Lifetime history of bruxism, snoring, intermittent poor sleep, and GERD Nocturnal bruxing events in subjects with sleep- symptoms. results indicate severe apnea. (22.) Incisal view dem- onstrates the damage from sleep bruxism and the erosive wear associated disordered breathing and control subjects. J with GERD and tongue position.(23.) Retracted tongue position in edentu- Craniomandib Disord. 1991;5:258-264. lous patients limits the available airway. Wearing their dentures at night may 22. Gold AR, Dipalo F, Gold MS, O’Hearn D. The allow for a more favorable airway. (24.) Many dentures worn at night demon- strate the same lateral wear facets indicative of the bruxism triad patient. A symptoms and signs of upper airway resistance fig. 24 complete history of bruxism, sleep, and GERD should be obtained. syndrome: a link to the functional somatic

40 inside dentistry | May 2010 | insidedentistry.net syndromes. Chest. 2003;123:87-95. 23. Guilleminault C, Stoohs R, Clerk A, et al. A cause of excessive daytime sleepiness: the up- per airway resistance syndrome. Chest. 1993; 104:781-787. quiz 24. Young T, Peppard PE, Gottlieb DJ. Epidemiology of : a Log on to www.insidedentistryCE.com to take this FREE CE quiz. population health perspective. Am J Respir Crit Care Med. 2002;165:1217-1239. 25. Shamsuzzaman ASM, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA. 2003; 290:1906-1914.

26. Redline S. Epidemiology of sleep-disor- dered breathing. Semin Respir Crit Care Med. 1998;19:113-122. 27. Lavigne GJ, Rompré PH, Montplaiser JY. Sleep bruxism: Validity of clinical research diagnostic criteria in a controlled polysom- nographic study. J Dent Res. 1996;75:546-552. 28. Lavigne GJ, Manzini C. Bruxism. In: Kryger M, Roth T, Dement W (eds). Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, Pa: W.B. Saunders Company; 2005:946-959. 29. van Selms MK, Lobbezoo F, Wicks DJ, et al. Craniomandibular pain, oral parafunctions, and psychological stress in a longitudinal case study. J Oral Rehabil. 2004;31:738-745. 30. Lavigne GJ, Guitard F, Rompré PH, Montplaisir JY. Variability in sleep bruxism activity over time. J Sleep Res. 2001;10:237-244. 31. Camparis CM, Formigoni G, Teixeira MJ, et al. Sleep bruxism and temporomandibular disorder: clinical and polysomnographic evalu- ation. Arch Oral Biol. 2006;51:721-728. 32. Kato T, Montplaisir JY, Guitard F, et al. Evidence that experimentally induced sleep bruxism is a consequence of transient arousal. J Dent Res. 2003;82:284-288. 33. Ohayon MM, Li KK, Guilleminault C. Risk factors for sleep bruxism in the general popula- tion. Chest. 2001;119:53-61. 34. Bader GG, Kampe T, Tagdae T, et al. Descriptive physiological data on a sleep brux- ism population. Sleep. 1997;20:982-990. 35. Oksenberg A, Arons E. Sleep bruxism related to obstructive sleep apnea: the effect of continuous . Sleep Med. 2002;3:513-515. 36. Kobayashi Y, Shiga H. The relationship between sleep apnea, bruxism, and the time it took the patient to seek for treatment in TMD patients. J Oral Rehabil. 2002;29:885. 37. Yoshida K. A polysomnographic study on masticatory and tongue muscle activity during obstructive and central sleep apnea. J Oral Rehabil. 1998;25:603-609. 38. Sjöholm TT, Lowe AA, Miyamoto K, et al. Sleep bruxism in patients with sleep-disordered breathing. Arch Oral Biol. 2000;45:889-896. 39. The Gallup Organization: A Gallup survey on heartburn across America. Princeton, NJ: Gallup; 1988. 40. Fass R, Dickman R. Clinical consequences of silent gastroesophageal reflux disease. Curr Gastroanterol Rep. 2006;8:194-200.

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Approved PACE Program Provider FAGD/MAGD Credit Approval does not imply acceptance by a state or provincial board of Program Approval for Continuing Education dentistry or AGD endorsement. 7/18/1990 to 12/31/2012 41. Shaheen N, RansohoffD F. Gastroesophageal continuing education Mail in answer form reflux, barrett esophagus, and esophageal cancer: scientific review.JAMA . 2002;287:1972-1981. Education efforts.We are pleased to offer you another avenue for obtaining 42. Lazarchik DA, Frazier KB. Dental erosion credits for your Continuing Education lessons. In addition to our FREE CE on our Web site, www.insidedentistryce.com, we are and acid reflux disease: an overview. Gen Dent. now offering a mail-in option to our readers who prefer to send in their tests for scoring. For a nominal fee of $28 ($14 per credit) 2009;57:151-156. to cover administrative and handling costs, your test will be graded and your certificate will be sent to you in the mail.S imply use 43. Campisi G, lo Russo L, Di Liberto C, et al. this page for your answers, fill it out completely, and send it along with your check or credit card information Saliva variations in gastro-esophageal reflux disease. J Dent. 2008;36:268-271. 44. Landry ML, Rompré PH, Manzini C, et al. Reduction of sleep bruxism using a mandibular advancement device: an ex- perimental controlled study. Int J Prosthodont. 2006;19:549-556. 45. Schönbeck AL, de Grandmont P, Rompré PH, Lavigne GJ. Effect of an adjustable man- dibular advancement appliance on sleep brux- ism: a crossover sleep laboratory study. Int J Prosthodont. 2009;22:251-259. 46. Gagnon Y, Mayer P, Morisson F, et al. Aggravation of respiratory disturbances by the use of an occlusal splint in apneic patients: a pilot study. Int J Prosthodont. 2004;17:447-453. 47. Arisaka H, Sakuraba S, Tamaki K, et al. Effects of wearing during sleep on the apnea-hypopnea index. Int J Prosthodont. 2009;22:173-177. 48. Guda N, Partington S, Vakil N. Symptomatic gastro-oesophageal reflux, arousals and sleep quality in patients undergoing polysomnog- raphy for possible obstructive sleep apnea. Aliment Pharmacol Ther. 2004;20:1153-1159. 49. Demeter P, Visy KV, Magyar P. Correlation between severity of endoscopic findings and apnea-hypopnea index in patients with gastro- esophageal reflux disease and obstructive sleep apnea. World J Gastroenterol. 2005;11:839-841. 50. Miyawaki S, Lavigne GJ, Mayer P, et al. Association between sleep bruxism, swallowing- related laryngeal movement, and sleep posi- tions. Sleep. 2003;26:461-465. 51. Ing AJ, Ngu MC, Breslin AB. Obstructive sleep apnea and gastroesophageal reflux.Am J Med. 2000;108:120S-125S. 52. Tawk M, Goodrich S, Kinasewitz G, Orr W. The effect of 1 week of continuous positive airway pressure treatment in obstructive sleep apnea patients with concomitant gastroesopha- geal reflux.Chest . 2006;130:1003-1008. 53. Dayyat E, Kheirandish-Gozal L, San Capdevila O, et al. Obstructive sleep apnea in children: rela- tive contributions of and adeno- tonsillar hypertrophy. Chest. 2009;136:137-144. 54. Noronha AC, de Bruin VM, Nombre e Souza MA, et al. Gastroesophageal reflux and obstruc- tive sleep apnea in childhood. Int J Pediatr Otohinolaryngol. 2009;73:383-389. 55. Zettergren-Wijk L, Forsberg CM, Linder- Aronson S. Changes in dentofacial morphology after adeno- in young children with obstructive sleep apnoea—a 5-year follow- up study. Eur J Orthod. 2006;28:319-326. 56. Knight DJ, Leroux BG, Zhu C, et al. A longitudinal study of tooth wear in orthodonti- cally treated patients. Am J Orthod Dentofacial Orthop. 1997;112:194-202.

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